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Microbiomes (bacteria, fungi, viruses etc...) are the substrate of all earthly organisms. From regulating soil and decay, to managing the environments on our skin and stomachs, the specific varieties and their ratios function in a whole host of methods to create the biological world in which we live.
Every human on the planet has a unique microbiomal fingerprint. It consists of the types of species and ratios of bacteria, fungi and viruses that live within and on our bodies. Though our microbiomal fingerprint make up does fluctuate throughout our lives (illness and age can both change it) it is quite stable in a healthy individual. To profile an individual's microbiomal fingerprint is an extremely complicated and lengthy process and although it can be done, it is a rare practice to carry out due to the cost and time the present methods require.
We obtain our microbiomal fingerprint primarily from our mother. The placenta is not sterile nor is the content and lining of the umbilicus. The mother passes portions of her normal microbiome (and abnormal microbiome should she have one) to her baby all throughout the term of her pregnancy.
None the less, the importance of human microbiomes has only relatively recently been discovered to be crucial to both individual and social well being.
An apt example of the immense importance of the microbiome to humans comes out of the investigations into probiotics carried out in the 90s. When people get infections that cannot be treated with standard strength antibiotics they are often given one or more stronger medications (Fortaz and Rifampicin for example are used to treat Methicillin-resistant Staphylococcus aureus - a particularly antibiotic resistant and nasty lesion forming bacteria). These high strength antibiotics whilst relatively selective, do damage and destroy large amounts of our normal microbiome (benign bacteria adhering to binding sites, or actively beneficial bacteria living in symbiosis with us). Once a person's microbiome is sufficiently disrupted they will become immuno-suppressed, unable to digest food correctly and consequently fatigued, this often leads to rapid weight loss and muscle depletion, they may incur liver damage and can even die due to complications and secondary diseases arising from these scenarios.
Early supplement treatments included regular regimens of probiotics. When tests are run to ascertain the efficacy of such regimens, they reveal low percentage improvement in patients and only marginally outperform placebos. The next option was testing mega-doses (much higher dosage short term courses) of probiotics. Whilst this type of supplement program was shown to have a higher efficacy than short term regular regimens of probiotics, some patients rejected the treatment as it irritated their already highly sensitive stomachs (mega-dosing is not recommended for healthy individuals, unless prescribed by a physician). For patients who fail to be ameliorated with these two treatments a third and final option is attempted. The treating doctor will request the patient (or family if the patient is unable to) to sign a permission form to conduct a fecal transplant. This is when a small sample of faeces from a patient's healthy parent is obtained and pneumatically inserted into the patient's stomach via a feeding tube. The faecies are then broken down by the patient's stomach. This reintroduces the normal microbiome of the parent to the patient.
The interactions of the disrupted microbiome and the reintroduced sample is one of competition and optimization. Our cells are able to recognize the constituents of our normal microbiome and actively promote those components whilst simultaneously fighting the foreign entities or normal but over grown cultures. However the mechanism is highly individual specific and most certainly more complicated, indeed scientists are still working on understanding microbiomal warfare. These fecal transplants have a relatively high success rate in those suffering from an unbalanced or severely depleted microbiome and saves lives.
Four quick notes:
1) Two recent studies conducted by KU Leuven University in Belgium revealed that people suffering from depression are also found to have to lack or relatively small populations of two common bacteria. It is hypothesized that these bacteria release an anti-inflammatory and assist in bio-site regulation and assist in fighting depression by aiding digestive function. This doesn’t necessarily mean that lacking these bacteria causes depression.
2) The majority of human smells are generated by bacterial processes and play a crucial role in pairing for humans. When you are assessing a potential mate smell plays a significant factor. Yet there are times when a partner may smell pleasing and mating may take place yet upon completing a successful coupling impregnation does occur. One of the reasons for this can be the male's ejaculate consisting of hostile bacteria/ substances that are rejected by the female's normal microbiome, and indeed another is the male's healthy ejaculate being rejected by female's hostile microbiome.
3) It was recently discovered that a deep-microbiome resides within the Earth's crust. Even the famous Kola bore hole revealed a deep-microbiome evidenced by trace irregularities at over 6 kilometers beneath the earth's surface. Whilst the age of the cultures cannot be determined, the age of the rocks can be. Some of the samples were dated at 2 billion years old.
4) It used to be thought that DNA held all the answers to inheritable traits yet these days the role of epigenetics (the study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself) has come to the forefront. The microbiome can radically change the processes of epigenetics and thus also plays a very important role in the functioning of inherit-ability.
As the human population of the planet in the age of the Anthropocene reaches its zenith of a predicted 11 billion individuals, antibiotics become less effective/ we are unable to discover new treatments and climate change exposes the planet to further unfamiliar conditions, the opportunity for dangerous bacteria, fungi and viruses to gain a foothold increases.
Everything from measles to ebola (see West African outbreak) to the common flu are already experiencing resurgences not seen in the last fifty years or if ever. These epidemics can follow somewhat regular cycles yet we are now entering unknown territory as the recent outbreaks have epidemiologists puzzled as to their size and speed of growth and hyper-concerned about the future of human immunity as they await the next worldwide contagion.
So why am I discussing this? Well, back in the late 80's I contracted a common flu virus that almost killed me. It left me with a weakened immune system and to this day I must be very careful about my lifestyle, diet and well being. Whilst we as humans see the macrobiota of the planet (plants, animals, lizards, birds etc...) as the 'real life' of Earth, the truth is we are all just extensions of the global microbiome. Indeed life on Earth for 90% of its existence was only the microbiome. It has actively decided to a very large degree what types of life have been able to flourish here on Earth.
I am happy it allowed me to live, may it also be kind to you in these coming years of great uncertainty.
  
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I agree. Bacteria super underrated. Thanks bacteria for all that you do.
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On June 05 2019 17:11 CHEONSOYUN wrote:
I agree. Bacteria super underrated. Thanks bacteria for all that you do.
Thank you 
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from what i know, things are way more complicated than "... but, but the microbiome".
this study, apart from its intention(show changes of the human gut microbiome induced by a fermented milk product) suggests that we don't really have the means to discover/measure/quantify all the changes in the git(gastrointestinal tract).The emergence of molecular tools based on the 16S rDNA gene brought about a revolution in understanding the immense diversity of gut microbial communities and their links with host health and diet. However, variations of 16S rDNA sequences do not provide basis for species-level resolution8. Consequently, studies using 16S gene as a phylogenetic marker and reporting unaltered gut microbiota upon probiotic consumption2,3,4,5,6 might have failed in detecting changes of the microbiota due to the lack of species-level resolution. Such hypothesis can be accurately studied now with the emergence of novel technologies allowing species-level gut microbiota mapping. basically we're limited by our tools.
you also need to take into account the structure and health of the whole digestive system from oral to rectal, since a problem in one can create a cascading effect in others: from oral infections, variation(hypo/hyper) in stomach PH values(vitamin/mineral absorption and the destruction of various bacteria/fungi/yeasts is PH based) , increased intestinal permeability, presence or absence of the appendices(it's hypothesized that it stores a very diverse bacterial flora that can repopulate the git after infections, antibiotics use, etc), the quantity/quality of bile or pancreatic enzymes, defects(inherited or acquired) in organs(bends, twists, varicated portions, etc), allergies, intolerances, the ratio of carbs to proteins to fats in ones diet, hormonal problems, etcetcetc.
you'd need a theory of everything here to even start diagnosing/standardizing/labeling states of normality.
and don't even get me started with vast power of the body to adapt to shortcomings(look at vegans: poor muscle development, accelerated aging, poor bone density, slower wound healing, oral health becomes compromised, bleeding gums and receding gum line, brittle hair, skin, and nails, cellulite, leaky gut and they keep going for decades); the adaptation is almost always in the bodys' detriment, but it gives it the ability to go on for a while.
that adaptation to stresses, also changes the body reaction/responsiveness to stimuli(probiotics in this case: some get sick from them, for some it has no effect, for others it's helpful).
Edit: worth a read, pretty exhaustive https://www.nature.com/articles/cmi20187?error=cookies_not_supported&code=edee0256-7311-4eb8-895a-c7e9235cb795 Perspectives and future directions
The commensal microbiome utilizes multiple pathways to shape mucosal immunity, and its impact may reach non-mucosal tissues and thus contribute to systemic autoimmunity in genetically susceptible individuals. The currently available techniques to detail the functions of the intestinal microbiome has provided more accurate information regarding the microbial changes in human autoimmune diseases. However, the scenario is complicated by the variability of the intestinal flora over short periods of time, which does not allow a historical perspective of the observed changes years after the initiation of the autoimmune process. Whether the observed changes are the cause or the consequence of the disease (or its treatment) remains enigmatic. Under this circumstance, several hypotheses have been proposed, aiming at explaining the causal link between the commensal microbiota and the development of diseases. Molecular mimicry, in which the gut microbiota may serve as a source of cross-reactive antigens that trigger autoimmune reactions, was postulated many years ago and is still being re-assessed and validated in different models9,10,96 Nevertheless, overwhelming data suggest a multifaceted effect of the microbiota on host physiology.165 In most cases, a perturbed microbiota may exacerbate the immune disorder in the setting of genetic susceptibility rather than ignite an initial autoimmune attack.
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I really like Oxalobacter formigenes, helping us not get kidney stones and gout as neonates. Thank you Oxalobacter!
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On June 05 2019 21:23 xM(Z wrote:from what i know, things are way more complicated than "... but, but the microbiome". this study , apart from its intention(show changes of the human gut microbiome induced by a fermented milk product) suggests that we don't really have the means to discover/measure/quantify all the changes in the git(gastrointestinal tract). Show nested quote +The emergence of molecular tools based on the 16S rDNA gene brought about a revolution in understanding the immense diversity of gut microbial communities and their links with host health and diet. However, variations of 16S rDNA sequences do not provide basis for species-level resolution8. Consequently, studies using 16S gene as a phylogenetic marker and reporting unaltered gut microbiota upon probiotic consumption2,3,4,5,6 might have failed in detecting changes of the microbiota due to the lack of species-level resolution. Such hypothesis can be accurately studied now with the emergence of novel technologies allowing species-level gut microbiota mapping. basically we're limited by our tools. you also need to take into account the structure and health of the whole digestive system from oral to rectal, since a problem in one can create a cascading effect in others: from oral infections, variation(hypo/hyper) in stomach PH values(vitamin/mineral absorption and the destruction of various bacteria/fungi/yeasts is PH based) , increased intestinal permeability, presence or absence of the appendices(it's hypothesized that it stores a very diverse bacterial flora that can repopulate the git after infections, antibiotics use, etc), the quantity/quality of bile or pancreatic enzymes, defects(inherited or acquired) in organs(bends, twists, varicated portions, etc), allergies, intolerances, the ratio of carbs to proteins to fats in ones diet, hormonal problems, etcetcetc. you'd need a theory of everything here to even start diagnosing/standardizing/labeling states of normality. and don't even get me started with vast power of the body to adapt to shortcomings(look at vegans: poor muscle development, accelerated aging, poor bone density, slower wound healing, oral health becomes compromised, bleeding gums and receding gum line, brittle hair, skin, and nails, cellulite, leaky gut and they keep going for decades); the adaptation is almost always in the bodys' detriment, but it gives it the ability to go on for a while. that adaptation to stresses, also changes the body reaction/responsiveness to stimuli(probiotics in this case: some get sick from them, for some it has no effect, for others it's helpful). Edit: worth a read, pretty exhaustive https://www.nature.com/articles/cmi20187?error=cookies_not_supported&code=edee0256-7311-4eb8-895a-c7e9235cb795 Show nested quote +Perspectives and future directions
The commensal microbiome utilizes multiple pathways to shape mucosal immunity, and its impact may reach non-mucosal tissues and thus contribute to systemic autoimmunity in genetically susceptible individuals. The currently available techniques to detail the functions of the intestinal microbiome has provided more accurate information regarding the microbial changes in human autoimmune diseases. However, the scenario is complicated by the variability of the intestinal flora over short periods of time, which does not allow a historical perspective of the observed changes years after the initiation of the autoimmune process. Whether the observed changes are the cause or the consequence of the disease (or its treatment) remains enigmatic. Under this circumstance, several hypotheses have been proposed, aiming at explaining the causal link between the commensal microbiota and the development of diseases. Molecular mimicry, in which the gut microbiota may serve as a source of cross-reactive antigens that trigger autoimmune reactions, was postulated many years ago and is still being re-assessed and validated in different models9,10,96 Nevertheless, overwhelming data suggest a multifaceted effect of the microbiota on host physiology.165 In most cases, a perturbed microbiota may exacerbate the immune disorder in the setting of genetic susceptibility rather than ignite an initial autoimmune attack.
Very fascinating!
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On June 06 2019 03:35 Uldridge wrote:
I really like Oxalobacter formigenes, helping us not get kidney stones and gout as neonates. Thank you Oxalobacter!
I did not know about that one! Thank you!
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On June 06 2019 03:35 Uldridge wrote:
I really like Oxalobacter formigenes, helping us not get kidney stones and gout as neonates. Thank you Oxalobacter! studies on vit.K (K2 - mk7 or mk8) show it as being involved in regulating soft-tissue calcification. Abstract OBJECTIVES: To provide a rational basis for recommended daily allowances (RDA) of dietary phylloquinone (vitamin K1) and menaquinone (vitamin K2) intake that adequately supply extrahepatic (notably vascular) tissue requirements. BACKGROUND: Vitamin K has a key function in the synthesis of at least two proteins involved in calcium and bone metabolism, namely osteocalcin and matrix Gla-protein (MGP). MGP was shown to be a strong inhibitor of vascular calcification. Present RDA values for vitamin K are based on the hepatic phylloquinone requirement for coagulation factor synthesis. Accumulating data suggest that extrahepatic tissues such as bone and vessel wall require higher dietary intakes and have a preference for menaquinone rather than for phylloquinone. RESULTS: At least some extrahepatic tissues including the arterial vessel wall have a high preference for accumulating and using menaquinone rather than phylloquinone. Both intima and media sclerosis are associated with high tissue concentrations of MGP, with the most prominent accumulation at the interface between vascular tissue and calcified material. This was consistent with increased concentrations of circulating MGP in subjects with atherosclerosis and diabetes mellitus. CONCLUSIONS: This is the first report demonstrating the association between MGP and vascular calcification. The hypothesis is put forward that undercarboxylation of MGP is a risk factor for vascular calcification and that the present RDA values are too low to ensure full carboxylation of MGP .Abstract Vitamin K is a composite term referring to a group of fat-soluble vitamins that function as a cofactor for the enzyme γ-glutamyl carboxylase (GGCX), which activates a number of vitamin K-dependent proteins (VKDPs) involved in haemostasis and vascular and bone health. Accumulating evidence demonstrates that chronic kidney disease (CKD) patients suffer from subclinical vitamin K deficiency, suggesting that this represents a population at risk for the biological consequences of poor vitamin K status. This deficiency might be caused by exhaustion of vitamin K due to its high requirements by vitamin K-dependent proteins to inhibit calcification. ... There are two forms of vitamin K: K1 (phylloquinone, PK) mainly found in green vegetables, and K2 (including different menaquinones, MKs) derived from intestinal bacteria and fermented food (cheeses and “natty”, a Japanese soybean product) [1,2]. Liver is also a rich source of menaquinones [3]. We know about more than 12 different types of MKs, from MK-4 to MK-15, but the most common MKs in humans are the short-chain MK-4; it is the only MK produced by systemic conversion of phylloquinone to menaquinones [4] .Because colonic bacteria synthesize a significant portion of the Vitamin K required for human needs, individuals with disruptions to or insufficient amounts of these bacteria can be at risk for Vitamin K deficiency. Newborns, as mentioned above, fit into this category, as their colons are frequently not adequately colonized in the first five to seven days of life. (Consumption of the mother's milk can undo this temporary problem.) Another at-risk population comprises those individuals on any sort of long-term antibiotic therapy, as this can diminish the population of normal gut flora .
Edit: thing is, as a general rule, people get the microbes/flora from the environment. your mother gives you a first dose(through milk, saliva and/or feces; needs natural birth and breastfeeding) then you diversify and establish it by eating foods, whole foods(fruits, veggies, free range animal meats); not sterilized, not pasteurized, uncooked, not waxed foodstuffs.
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Edit: thing is, as a general rule, people get the microbes/flora from the environment. your mother gives you a first dose(through milk, saliva and/or feces; needs natural birth and breastfeeding) then you diversify and establish it by eating foods, whole foods(fruits, veggies, free range animal meats); not sterilized, not pasteurized, uncooked, not waxed foodstuffs.
Our houses are also fantastic examples of microbes regulating an environment and attaching to us. Cultures grown from samples taken from peoples' beds can be kaleidoscopic in variety.
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https://mpkb.org/home/pathogenesis/microbiota great resource for some "did you know ..." tidbits plus research trends, novelties, insights and the likes; it's part of the NIH Human Microbiome Project, https://hmpdacc.org Antibiotic resistant strains predate human discovery of antibiotics – In a 2011 Nature study (press release), researchers carefully dug ancient 30,000 year old permafrost sediments out of the Canadian Northwest and sequenced the bacterial DNA found in it.20) The team concluded that antibiotic resistance genes predate our use of antibiotics and offers the first direct evidence that antibiotic resistance is an ancient, naturally occurring phenomenon widespread in the environment. This should not be surprising especially when one considers that penicillin came from a mold, tetracycline and demeclocycline from a strep mutant while Vancomycin came from Amycolatopsis orientalis.
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Communities of people have distinctive mixes of microbes – Two human ethnic groups based in India, which could not be distinguished on the basis of human DNA markers, could be distinguished based on their patterns of H. pylori variation.22)
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At least in fruit flies, gut microbes can alter mating preferences – In a 2010 study, mating preference was achieved by dividing a population of Drosophila melanogaster and rearing one part on a molasses medium and the other on a starch medium. When the isolated populations were mixed, “molasses flies” preferred to mate with other molasses flies and “starch flies” preferred to mate with other starch flies. The mating preference appeared after only one generation and was maintained for at least 37 generations. Antibiotic treatment abolished mating preference, suggesting that the fly microbiota was responsible for the phenomenon.36) Athogenic bacteria have a variety of ways of disrupting the activity of and causing damage to human genes.
Horizontal gene transfer – Bacteria can insert their DNA into human DNA.
Interruption of transcription and translation of DNA and RNA – Intracellular pathogens, which inhabit the cytoplasm, can interfere with the steps involved in the transcription and translation processes. Such interference results in genetic mutations, meaning that human DNA is almost certainly altered, over time. The more pathogens people accumulate, the more their genome is potentially altered.
Disruption of DNA repair mechanisms – Since environmental factors such as exposure to ultraviolet light result in as many as one million individual molecular lesions per cell per day, the potential of intracellular bacteria to interfere with DNA repair mechanisms also greatly interferes with the integrity of the genome and its normal functioning. If the rate of DNA damage exceeds the capacity of the cell to repair it, the accumulation of errors can overwhelm the cell and result in early senescence, apoptosis or cancer. Problems associated with faulty DNA repair functioning result in premature aging, increased sensitivity to carcinogens, and correspondingly increased cancer risk.
Lifelong persistent symbiosis between the human genome and the microbiota [the large community of chronic pathogens that inhabit the human body] must necessarily result in modification of individual genomes. It must necessarily result in the accumulation of ‘junk’ in the cytosol, it must necessarily cause interactions between DNA repair and DNA transcription activity. Trevor Marshall, PhD
The highly variable range of human genetic mutations induced by bacteria have been identified with some success by researchers with the Human Genome Project. Rather than serving as markers of particular diseases, such mutations generally mark the presence of those pathogens capable of affecting DNA transcription and translation in the nucleus. from a link referral.
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EPT
